CARDIAC
OUTPUT,VENOUS
RETURN AND THEIR
REGULATION.
DR.HAROON RASHID.
 OBJECTIVES
•
•
•
Define Stroke volume, Cardiac output
Venous return ,& identity their normal
values.
Describe control (intrinsic & extrinsic) of
Cardiac output & Venous return.
Enumerate the causes of high & low
cardiac output states.
 Cardiac Output
 Def: Volume of blood pumped
out by each ventricle per minute (
i.e minute output/ventricle)
 Normal value: 5L / min. (i.e RV
pumps 5L/min to lungs & same
time LV pumps 5L/min to aorta )
 Cardiac Index: CO/Sq.mt.body
surface area/min
Normal value: 3.5L/Sq.mt/min.
Significance of CI: It is a better
parameter for comparing CO of
the people of same age and sex.
 CO
 Distribution: at rest
Brain = 750 ml / min.
Heart = 250 ml / min.
Liver = 1500 ml / min.
5L /min
Kidneys =
1200ml/min
(From LV)
ml/min
Muscle = 800
Skin&others=500ml/min
5L / min
( From RV)
Pulmonary
circuit
 Factors determining Cardiac
Output:
CO is a product of SV and HR
CO =
X
70ml / min X 75
bpm
= 5L / min.
 Stroke Volume : It is the volume of blood pumped by
each ventricle per beat.
 Normal Values=70ml to 90ml.
 Stroke Volume =End Diastolic
Volume-End Stroke
volume.
 Venous Return.
 Def:- Volume of blood returning
from systemic circulation to heart.
 Any factor/condition increases
venous return increases End
diastolic volume.
 Factors determining
 Venous return
 Ventricular compliance
 Duration of ventricular diastole
 Atrial systole.
Factors determining venous return:
 Blood volume
 Gravity
 Pressure gradient
 Negative intrapleural pressure
 Valves of veins
 Muscular pump
Increased venous return
EDV increases
Force of Contraction increases
Stroke volume increases
Cardiac output increases.
Factors determining
Stroke Volume.
 Starling’s law of heart
 Def: Force of contraction of
myocardium is
directly proportional to the
initial
length of muscle fiber
within
physiological limits.
 In heart : When EDV increases
Stroke volume increases
(EDV stretching of vent. Initial
length FC )
 Starling’s law
 Molecular basis
 When initial length of muscle is
increased. The sarcomere length
increases Increased number
cross linkages are formed
force
of contraction
 Importance of Starling’s
law in heart
1.An increase in venous return to the
heart increases ventricular EDV
(preload) and the force of
ventricular contraction, which
enables the heart to eject the
additional blood that was returned
to it. Conversely, a decrease in
venous return leads to a decrease in
SV by this mechanism.
 Importance of Starling’s
law in heart
2. To match the stroke volumes of
two ventricles so exactly that
neither a stagnation ( pulmonary
edema ) not total emptying of the
pulmonary circulation can occur.
As both of them are fatal
Force – frequency relation:
When frequency = HR increases,
for initial few beats, the force of
contraction increases due to
increased ca2+ availability (
Beneficial effect )
 HEART RATE
The rate at which heart beats / min.
Normal range: 60 - 80 beats/min.
< 60 bpm =
Bradycardia
> 100 bpm =
Tachycardia.
Method of study:
1.Examination of arterial pulse(eg
Radial)
2.Auscultation of heart sounds by
stethoscope.
3.ECG
 Factors determining HR
 Age :New borns, Old age increases.
 Sex :Slightly more in females than
males.
 Body temperature, Posture, Emotions,
Respiration it increases.
 Hormonal influences: - Adrenaline,
NA, Thyroxine, Vasopressin.
 Factors determining HR
 Neuronal influences:- Central
nervous system & Peripheral
Nervous System
 Cardio Vascular reflexes:

- Baro receptor reflex

- Chemoreceptor reflex

- Bain-Bridge reflex

- Cushing’s reflex.

-Bejold-Jarisch reflex.
 Influences from higher centers: -
VMC, CIC,

Hypothalamus,
- Limbic system
 Factors determining HR
 Age :New borns, Old age increases.
 Sex :Slightly more in females than
males.
 Body temperature, Posture, Emotions,
Respiration it increases.
 Hormonal influences: - Adrenaline,
NA, Thyroxine, Vasopressin.
 Factors determining HR
 Neuronal influences:- Central







nervous system & Peripheral
Nervous System
Cardio Vascular reflexes:
- Baro receptor reflex
- Chemoreceptor reflex
- Bain-Bridge reflex
- Cushing’s reflex.
-Bejold-Jarisch reflex.
Influences from higher centers: VMC, CIC,

Hypothalamus,
- Limbic system
 Heart Rate.
 Age Vs HR: Infants: 140 – 150 bpm.
Adults: 60 – 80 bpm.
Decline in HR during aging is due to increase in
vagal tone.
 BSA Vs HR: HR 1/α BSA.
 Sex Vs HR: Females have higher HR than males of
same age, due to: sympathetic tone/ vagal tone /
BSA/ BP.
 Emotion & HR: Anger, Anxiety: HR( Sympathetic
tone)
Shock, Grief: HR ( Vagal. Tone)
 BT & HR: for every rise in 10C: HR by 20bpm.
10 F: HR by 10 bpm.
 HR
 Posture & HR: Lying down to
standing: HR due to
Mary’s law.
 Respiration & HR: HR increases
during inspiration &
HR decreases
during expiration
= Sinus
arrhythmia.
discharge of inspiratory
center spill over
vagal nucleus and cause
inhibition vagal tone
HR
 Barometric pressure & HR: Increase
barometric pr.
HR,
High
altitude: barometric pressure
HR
 Factors affecting/modifying CO
 Age
 Sex: Male- more, Female – less
CO
 Exercise: Increases, from 5L/min
to
25 L / min & 35L
/min(athletes)
 Emotion: Anxiety, anger ,
Depression
 Pregnancy: CO increases due to
in Blood Volume by 30%
 Posture: Lying to standing, CO
20-30%
 Sleep: CO
Why Measure Cardiac
Output?
 Why Measure Cardiac Output?
 The
reasons for determining
cardiac
output
are many, including: checking for
arterial
blockage, determining efficiency
of
the
heart
pump, determining mean vascular
pressure,
and diagnoses of various inlet
impedance
problems,
including
microstenosis,
venous
obstruction, atrial fibrilation,
cardiac
tamponade, ventricular non-
compliance,
extremely rapid heartrate.
and
 Methods of measurement CO
 1. Fick’s Principle.
 2. Dilution technique.

- a. Dye dilution – T1824,






Indocyanin green
- b. Thermo dilution – cold
saline
- c. Isotope dilution – P32,
I131
3. Ballistocardigraphy.
4. Echocardiography with dopler.
5. X ray cardiometry.
6. Electromagnetic flow meters ( in
animals )

Fick Principle
Def: Amount of sub ( x ) taken up or
given out by an organ is equal to
arterio-venous difference of that
substance times blood flow.
Qx = ( Ax – Vx ) X Blood flow.
This can be modified as:
Blood flow = QX = ml / min.
Ax - Vx
 CO
BF of Rt.Vent. = BF of
Lt.Vent. = CO
 Hence Pulmonary blood flow is
determined as follows:
 Sub. = O2, Organ = Lungs.
 Qx = 250 ml / min.
 Ax = 21ml / min ( Arterial O2%)
 Vx = 16 ml / min ( Pul.artery’s blood
sample is collected by cardiac
catheterization )
 Now BF ( CO ) = 250 / 21-16 X 100 = 5L /
min.
 Disadvantage: As cardiac
catheterization can not be done during
exercise, CO during exercise can not be
measured.
 Applied aspect of CO
 Low CO is seen in:
* Myocardial Infarction
* Congestive cardiac failure
* Complete heart block
* Atrial fibrillation
* Pericardial effusion
 High CO is seen in:
* Thyrotoxicosis
* Cushing’s syndrome
* Anaemia.
 Objectives /summary
At the end of this session, the
student should be able to :
• Define Cardiac Output,Stroke
volume,Venous return with its
normal values.
• Describe the mechanism of
regulation of Cardiac output.
• Name the diseases in which
Cardiac output increases &
decreases.
 References:Guyton & Hall,Text book
of Physiology,12th edition.Page 229234.
 Ganong,24 th edition.
 Internet.